[Epidemiology of yellow fever in Central Africa].
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Biomedical subjects
Publications and source records attributed to G T Werner.
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Infections with Entamoeba histolytica do not necessarily cause disease in those infected. The parasite may act as commensal (cysts living in the bowel) or it may cause a broad spectrum of clinical illness. Some of the factors causing overt disease are poorly understood. An acute amebic dysentery is accompanied by bloody stools, abdominal pain and indigestion. The most important extraintestinal complication of an amebic infection is a liver abscess causing severe pain, fever, nausea and vomiting. The diagnosis of an amebic infection is based upon isolation of the parasite from the stools. Extraintestinal amebiasis is diagnosed - apart from the clinical picture - by serology. For treatment of intestinal amebiasis so-called contact-amebicides can be recommended. An amebic abscess of the liver usually responds well to dehydroemetine, metronidazole or any other derivative or imidazole and chloroquine. Surgical treatment of amebic liver abscess is only required if complications arise.
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The outcome of viral infection appears to be the result of a complex interplay of both viral and host factors. The virus-host cell relationship as well as the host's immune response are the major factors determining the type of infection and the expression of the disease. Demyelination disease appears to be rare complication of a systemic viral infection. The mayor factor in its expression is an altered response to the virus favoring the establishment of a noncytocidal abortive infection of the glial cells, which in turn induce a complex of potentially pathogenic immune mechanisms.
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If rabbits were given total body irradiation and infected wih vaccinia virus (strain Elstree) a severe disease developed with a viraemia lasting up to 12 days. The clearance of the virus from the peripheral blood was severely impaired by x-ray doses above 800 R. The attenuated vaccinia virus strain MV did not turn virulent, if it was injected to irradiated rabbits. With caution it can be assumed that live vaccines, containing attenuated viruses, may be given to immunosuppressed persons. Rats are not susceptible to ectromelia-virus (mouse-poxvirus); overt clinical sympatoms, however, with a mortality of 30 per cent developed in irradiated rats. This proofs that specific poxviruses can be transferred to another species. As the experimental conditions are unnatural, this may occur only rarely in immunosuppressed persons. After intracerebral infection of Balb-C-mice with low doses of vaccinia virus two types of infection were seen: 1. a severe cytocidal infection of leptomeninges, chorioid plexus and vessels; 2. a noncytocidal, latent infection of glial cells and neurons. Several animals developed a picture resembling experimental allergic encephalomyelitis. It seems that irradiation altered the antigenic conditions of the cytoplasmic membranes in non-cytocidally infected cells. The model might explain some processes in the pathogenesis of demylinating diseases.
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A combined traumatism adversely affects radiation disease. Therefore it was of interest to investigate what influence exerts a combined lesion on an existing immunity state. After whole-body irradiation alone as well as after combined irradiation and traumatism, no significant decrease of the antibody level was found in rabbits which had been infected with vaccina virus Elstree four weeks before the irradiation. The conclusion seems justified that patients submitted to a therapeutic immunosuppression have to be vaccinated against dangerous virus infections before and that a natural immunity or an immunity induced by vaccination cannot be destroyed even by an accident involving a high radiation exposure.
Pretreatment with BCG yielded a high degree of protection against experimental vaccinia virus infections in mice. Corynebacterium parvum and Aristolochia acid were less protective; other immunostimulants were ineffective.